Although electric countershock is the treatment of choice for many atrial arrhythmias and is the only treatment available for the termination of ventricular fibrillation (sudden cardiac death), many recent reports have shown that dose-dependent injurious side effects result. In previous studies, we have shown that this post-shock dysfunction is related to a prolonged depolarization of the myocardial cell membrane and to a possible calcium overload. This work also indicated that the mechanisms producing post-shock dysfunction differ from those producing defibrillation, thus suggesting that the dysfunction can be minimized without sacrificing defibirillating efficacy. In the present study, we will utilize photocell mechanogram and intracellular micro-electrode techniques in "adult-type" cultured myocardial cells to examine in greater detail the mechanisms underlying post-shock dysfunction at the cellular level. We will determine the role of specific parameters of the defibrillating waveshape (e.g., peak voltage energy, slope of the waveform) in altering the ratio between dysfunction producing and defibrillation threshold-shock intensities (the "safety factor" of the waveshape). We will also determine the mechanisms through which multiple shocks given at closely spaced intervals potentiate myocardial damage and the differing sensitivity of the cell to the shock when it is given in various phases of the cardiac excitation cycle. The results of these studies will be incorporated into theoretical models to explain the defibrillation and the injury-inducing processes in terms of dynamic membrane characteristics and electromagnetic field theory. The results of these studies are expected to suggest specific modifications in counter-shock procedures which are based on a firm physiological understanding of the actions of the strong electric field on the myocardial cell. In addition to yielding information of potentially significant clinical interest, these studies will also increase our understanding of the fundamental mechanisms underlying the interactions of external electric fields with biological systems.